The hydrocephalus syndrome still today represents a complex and difficult challenge both as regards understanding the pathogenetic mechanisms which are at the origin thereof and as regards the identification and the implementation of the best methods of possible treatment.
Numerous pathogenetic hypotheses of hydrocephalus have been put forward over recent decades.
For completeness of information, the hypotheses that have gained and currently gain the greatest consensus will be described in brief here below.
Hypothesis of the “Circulation” of the Cerebrospinal Fluid
The first hypothesis which is also that currently most followed and accepted, is based on the assumption of a “circulation” of the cerebrospinal liquid or liquor starting from the choroid plexuses of the cerebral ventricles and with final target at the Pacchionian granulations of the cerebral convexity.
According to this hypothesis one obstacle to this “circulation” placed at any level and with any means, caused for example by acqueductal stenosis, a tumour of the posterior cranial fossa, a reduction in absorption as a result of haemorrhages or infections in the subarachnoid spaces, is at the origin both of so-called “obstructive” or “non-communicating” hydrocephalus and of the “non-obstructive” or “communicating” type.
Leaving aside, as well as considerations of a theoretical nature, a numerous series of indirect and experimental data contrary to the pathogenetic hypothesis of an obstacle to the flow of liquor, that which brought down this hypothesis definitively was the “direct” evidence, in the animal and human model, of the lack of a “circulation” of the cephalorachidian liquid, at least in the form wherein it should be in action for a mechanism of “obstacle” to this circulation to be able to produce a significant ventricular dilation.
In other words it has been extensively demonstrated, on the one hand, that a “diffusion” exists and not a displacement of volume (i.e. a “circulation”) of the liquor inside the intracranial system, in such a way that the same sites of production of the liquor are also assigned its absorption and, on the other hand, the movement of the liquor inside and outside the ventricular cavities is made up of a periodical oscillation synchronous with the heartbeat, but “without” a real “clear flow” in one direction or in the other.
This conclusion is reached also by extensive medical literature on the subject, supported by experimental data, bearing in mind that the fundamental variable to be considered, in the analysis of these data, is always the “rate” of the flow, i.e. the so-called “signal void”.
In fact the item of data obtained with experimental measurement has to be appropriately corrected so as to take account of the variation in calibre of the structure (usually the aqueduct of Sylvius) in which the measurement is taken, which, as is known, periodically thins in systole, thus causing an increase in the speed (but not of the flow) and widens in diastole, thus causing an opposite effect such as to compensate exactly the previous one, thus reconfirming the lack of a “clear flow” and, therefore, of a real “circulation” of cerebrospinal fluid (CSF).
Hypothesis of “Ventricular Pulsatility”
The second hypothesis is based on the observation that a condition of hydrocephalus, both clinical and experimental, is very often associated with an increase in the so-called “CSF pulsatile pressure”, i.e. in the difference between the maximum value and the minimum value of the intracranial pressure during every cardiac cycle.
Going into depth as regards this second hypothesis, on the basis of a model of intracranial system with rigidly constant volume, a different explanation can be put forward for the onset of the hydrocephalus syndrome, for which the development of the hydrocephalus, of whatever type it is, irrespective of its aetiology, is produced by the association between the “intraventricular pulsatility of the choroid plexuses” and an “asymmetric response” of the brain parenchyma.
In particular this second hypothesis take account of a behavioural feature well known in literature as regards “visco-elastic” substances, to which the brain parenchyma has always been compared on the anatomic-structural level.
This means that the brain, with respect to the actual pulsating force acting thereon, is more easily “compressible” (in systole) than it is “distensible” (in diastole) at the end of the phase of compression.
The continuing alternation between systole (compression) and diastole (distension) causes a progressive reduction in the volume of the brain, and therefore an increase in the ventricular volume, up to a new point of equilibrium between the forces acting in the two directions which will determine the current dimensions of the cerebral ventricles, from normal or relatively normal volumes up to the extreme degrees of the hydrocephalus syndrome.
From what has been disclosed it is clear how the systems of treatment of hydrocephalus currently in use and based, fundamentally, on the use of so-called “CSF shunts”, i.e. on the displacement of part of the CSF volume from the intracranial system towards other cavities of the body, cannot correspond, except partially, indirectly and inaccurately, to the solution of the pathogenetic alteration, as hypothesised here.
This incongruity clearly explains, moreover, the limitations still present in the traditional treatment of hydrocephalus syndrome.
A radical solution to the problem appears possible only by acting on one of the two factors, or both, which were illustrated previously, i.e. the “intraventricular pulsatility” and the “asymmetric response” of the brain parenchyma.
Reference to Previous Patent Applications Designating the Same Inventor
In the same field of the present invention, i.e. of the treatment of hydrocephalus syndrome and the devices which can be used in this treatment, mention is made of the following two previous patent applications, both designating the same inventor as the current patent application:                No. RM2006A00592, filed on 2 Nov. 2006 and granted with No. 0001372554, entitled “IMPLANTABLE DEVICE FOR THE TREATMENT OF HYDROCEPHALUS SYNDROME” and        No. MI2012A000097 of 27 Jan. 2012, entitled “IMPROVED IMPLANTABLE DEVICE FOR THE TREATMENT OF HYDROCEPHALUS SYNDROME AND CORRESPONDING METHOD”.        
These two previous patent applications, basing on the context previously set out and on the various hypotheses, in particular the second, “which were formulated to justify the treatment adopted for hydrocephalus syndrome, propose a rotary volumetric micro pump which, appropriately actuated, removes liquor from the cranial site and moves it into an accumulator, when it is necessary to reduce the actual value of the intracranial pressure or ICP, and reintroduces it into the cranial site when it is instead necessary to increase the instantaneous value thereof.
The systems described in these previous patent applications refer to and comprise, as an essential part, electric devices with electronic components.
The present patent application is instead aimed at a system or device suitable for obtaining the same benefit of treatment of hydrocephalus by means of the use of exclusively mechanical devices, therefore without the use of electric or electronic parts.